Department of Biochemistry and Molecular Biology, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA.
Department of Anatomy and Neurobiology, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA.
Glia. 2020 Jul;68(7):1513-1530. doi: 10.1002/glia.23799. Epub 2020 Feb 17.
The generation of fully functional oligodendrocytes, the myelinating cells of the central nervous system, is preceded by a complex maturational process. We previously showed that the timing of oligodendrocyte differentiation and rat brain myelination were altered by perinatal exposure to buprenorphine and methadone, opioid analogs used for the management of pregnant addicts. Those observations suggested the involvement of the μ-opioid receptor (MOR) and the nociceptin/orphanin FQ receptor (NOR). However, it remained to be determined if these receptors and their endogenous ligands could indeed control the timing of myelination under normal physiological conditions of brain development. We now found that the endogenous MOR ligand endomorphin-1 (EM-1) exerts a striking stimulatory action on cellular and morphological maturation of rat pre-oligodendrocytes, but unexpectedly, these effects appear to be restricted to the cells from the female pups. Critically, this stimulation is abolished by coincubation with the endogenous NOR ligand nociceptin. Furthermore, NOR antagonist treatment of 9-day-old female pups results in accelerated brain myelination. Interestingly, the lack of sex-dependent differences in developmental brain levels of EM-1 and nociceptin, or oligodendroglial expression of MOR and NOR, suggests that the observed sex-specific responses may be highly dependent on important intrinsic differences between the male and female oligodendrocytes. The discovery of a significant effect of EM-1 and nociceptin in the developing female oligodendrocytes and brain myelination, underscores the need for further studies investigating brain sex-related differences and their implications in opioid use and abuse, pain control, and susceptibility and remyelinating capacity in demyelinating disease as multiple sclerosis.
少突胶质细胞是中枢神经系统的髓鞘形成细胞,其成熟过程十分复杂。我们之前的研究表明,围产期接触丁丙诺啡和美沙酮(用于治疗孕妇成瘾的阿片类药物类似物)会改变少突胶质细胞的分化和大鼠脑髓鞘形成的时间。这些观察结果表明μ-阿片受体(MOR)和孤啡肽/孤啡肽受体(NOR)参与其中。然而,仍需要确定这些受体及其内源性配体是否可以在正常生理条件下控制髓鞘形成的时间。我们现在发现,内源性 MOR 配体内吗啡肽-1(EM-1)对大鼠前少突胶质细胞的细胞和形态成熟具有显著的刺激作用,但出乎意料的是,这些作用似乎仅限于雌性幼鼠的细胞。关键的是,这种刺激会被内源性 NOR 配体孤啡肽共同孵育所消除。此外,9 日龄雌性幼鼠的 NOR 拮抗剂处理会加速大脑髓鞘形成。有趣的是,EM-1 和孤啡肽在发育中大脑中的性别依赖性差异或 MOR 和 NOR 在少突胶质细胞中的表达缺乏差异表明,观察到的性别特异性反应可能高度依赖于雄性和雌性少突胶质细胞之间的重要内在差异。EM-1 和孤啡肽在发育中的雌性少突胶质细胞和脑髓鞘形成中具有显著作用的发现,突显了进一步研究大脑性别差异及其在阿片类药物使用和滥用、疼痛控制以及多发性硬化症等脱髓鞘疾病中的易感性和髓鞘再生能力方面的意义的必要性。